Table of Content

Volume 24 Issue 12
26 December 2019

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Role of RAB32 on proliferation and migration of chronic myeloid leukemia K562 cells

BAO Jing，LI Xiaofeng，ZHANG Hanshuo，XU Qingqing，MENG Xiaoming，HUANG Cheng，LI Jun

2019, 24(12):  1321-1327.  doi:10.12092/j.issn.1009-2501.2019.12.001

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AIM: To investigate the effects of RAB32 on the proliferation and migration of chronic myeloid leukemia (CML) K562 cells. METHODS: The expression of RAB32 in newly diagnosed CML patients, healthy volunteers and K562 cell lines were assessed using Western blot and qRT-PCR. In addition, RAB32 gene expression was knocked down using RAB32-shRNA, and then the cell cycle variation of K562 cell was analyzed by flow cytometry. The expressions of cell proliferation-related genes (C-myc and CyclinD1) and migration-associated genes (MMP-3 and MMP-9) were assessed using Western blot and qRT-PCR. RESULTS:The results of Western blot and qRT-PCR showed that RAB32 were highly expressed in both CML patients and the K562 cell line (P＜0.01). Cell cycle analysis showed that compared with NC-shRNA group, the RAB32-shRNA group had decreased proportions of S-phase and G2/M-phase, especially S-phase cells (P＜0.01). The protein levels of C-myc, Cyclin D1, MMP-3 and MMP-9 were significantly down-regulated in K562 cells transfected with RAB32-shRNA compared with NC-shRNA group (P＜0.01). The mRNA levels of these four factors were also reduced in RAB32-shRNA group compared to NC-shRNA group (P＜0.01). CONCLUSION: Down-regulation of RAB32 could weaken K562 cell proliferation and migration.

miR-142-5p inhibits proliferation and migration of gastric cancer cells through DNMT1

LI Yuqin, WANG Kai, AO Li, LU Xiaolan, SHI Jianping

2019, 24(12):  1328-1334.  doi:10.12092/j.issn.1009-2501.2019.12.002

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AIM: To investigate the role of miR-142-5p in gastric cancer（GC） cells and its mechanism. METHODS: The expression of miR-142-5p was detected by qRT-PCR; the effects of microRNA-142-5p on cell proliferation and migration were studied by CCK8 and Transwell assays; and the target of miR-142-5p was confirmed by dual luciferase reporter assay gene and Western blot assays. RESULTS:The expression of miR-142-5p in GC tissue and cell line was lower than that in normal gastric tissues and GES-1 cells, and the expression level of miR-142-5p was closely related to tumor size and lymph node metastasis. Overexpression of miR-142-5p in MKN28 cells and silencing miR-142-5p in BGC-823 cells inhibited and promoted the proliferation and migration of gastric cancer cells, respectively. DNA methyltransferase 1 (DNMT1) was the direct target of miR-142-5p, which could directly be regulated by miR-142-5p, and miR-142-5p regulated the proliferation and migration of gastric cancer cells through DNMT1. CONCLUSION: miR-142-5p is decreased in GC, implying an anti-oncogenetic effect to inhibit the proliferation and migration of gastric cancer cells by inhibiting DNMT1.

Human umbilical cord-derived mesenchymal stem cells alleviate adjuvant arthritis by regulating macrophage in vitro

CHENG Run, DING Wenxi, YAN Shangxue, WEI Wei

2019, 24(12):  1335-1340.  doi:10.12092/j.issn.1009-2501.2019.12.003

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AIM: To study the effect and mechanism of the human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) on the function of rat macrophages in vitro. METHODS: Peritoneal macrophages were isolated from rats with adjuvant arthritis (AA) at 28-30th days and co-cultured with hUC-MSCs（1∶1,1∶5,1∶10,1∶50）for 48 hours.The phagocytic ability of rat macrophages was detected by phagocytosis neutral red method;the percentage of macrophage subtype was detected by flow cytometry;the TNF-α, IL-1β,IL-6 and IL-10 levels in culture supernatant were detected by ELISA.RESULTS:After co-culturing hUC-MSCs (1∶10,1∶5,1∶1) with Mφ,the percentage of M2 macrophages increased significantly ［(34.0±2.6)%，(33.0±1.9)%，(47.0±7.3)% vs. (24.0±1.9)%］(P<0.01),the percentage of M1 macrophages decreased significantly［(31.0±2.5)%，(30.0±2.7)%，(30.0±1.9)% vs. (39.0±7.1)%］(P<0.01),and the average M2/M1 ratio increased with the number of co-cultured hUC-MSCs cells (1.2±0.1,1.2±0.2,1.5±0.2 vs. 0.8±0.1) (P<0.05);Compared with the model group,co-cultivation of hUC-MSCs with different ratios (1∶50, 1∶10,1∶5,1∶1) and Mφ can also significantly reduce the phagocytic index of Mφ(2.10±0.18,2.00±0.16, 1.50±0.11,1.40±0.11 vs. 2.4±0.20) (P<0.05),significantly reduced the levels of TNF-α((143.0±15.0),(128.0±12.0),(95.0±8.5), (44.0±5.9) pg/mL vs. (157.0±14.0) pg/mL)) (P<0.01),IL-1β((70.0±9.9), (66.0±5.9),(54.0±5.2),(41.0±6.4) pg/mL vs. (84.0±12.0) pg/mL)(P<0.01) and IL-6 ((95.0±5.8),(73.0±4.5), (65±5.1),(52.0±4.7)pg/mL vs. (109.0±7.6) pg/mL)(P<0.01),promoting IL-10 secretion ((228.0±34.0), (445.0±55.0),(568.0±49.0),(858.0±77.0) pg/mL vs. (85.0±14.0) pg/mL)(P<0.01).CONCLUSION: hUC-MSCs could regulate the function of AA rats macrophage in vitro with inhibition of the polarization and the phagocytosis, restoration the balance of pro-inflammatory and anti-inflammatory cytokines level.

Timed dose-response relationship of pain in autistic model rats

YANG Liqin, LI Zhiyu, TAN Pei, XU Wenting, ZHANG Zhongnan, WANG Mengya

2019, 24(12):  1341-1346.  doi:10.12092/j.issn.1009-2501.2019.12.004

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AIM: To observe the characteristics of timed dose-response relationship (TDRR) of pain in autistic model rats. METHODS: Ten pregnant SD rats were randomly divided into model pregnant group (n=6) and normal pregnant group(n=4). The model pregnant group rats were prepared by intraperitoneal injection of sodium valproate 600 mg/kg at 12.5 days after pregnancy and equivalent volume of saline was used as control injection in normal pregnant group.Then their offspring were used as model group (n=24) and normal group (n=22),respectively.During the period of 35 days after birth, a series of behavior tests were measured to identify the autistic model rats. Thereafter, the paw withdrawal mechanical threshold (PWMT) and tail flick latency (TFL) evoked by light radiant heat were measured from these rats in two groups.RESULTS:The growth and development indicators and the ability of behavioral exploration in model group rats were both less than those in normal group (P<0.01).Compared with normal group rats,the PWMT of the model group rats increased significantly (P<0.01).TFLs of rats in two groups were both shortened with increased light intensities, indicating a hyperbolic type-like TDRR. However, the TFLs in the TDRR curve of model group rats were longer than those of normal group rats(P<0.01). CONCLUSION: These preliminary results suggest that the autistic model rats increase the threshold of mechanical and heat pain, and change the TDRR curve of TFL to right either.

Novel compound HYY-002 inhibits paroxysmal atrial fibrillation in rats

YANG Leixi, FENG Kai, FAN Xueting, WEI Yanchun, LIU Tingting, TANG Yiqun

2019, 24(12):  1347-1352.  doi:10.12092/j.issn.1009-2501.2019.12.005

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AIM:To investigate the inhibitory effect of HYY-002 on atrial fibrillation(AF). METHODS:Male SD rats were randomized into 5 groups:normal,model,amiodarone(30 mg/kg,i.p.), low-dose and high-dose HYY-002 group. The rats were administrated Ach-CaCl2 (i.v.) for 10 days to establish rat AF model. From the 4th day, rats in treatment group were treated with amiodarone (30 mg/kg, i.p.) and HYY-002 (2 mg/kg, 10 mg/kg, i.g.) 1 hour before modeling. AF duration and ECG parameters were measured every day. On the 11th day, AERP of every rat were measured and the inflammatory cytokines and miR-135a in plasma were detected. RESULTS:In the model group, AF duration increased persistently and AERP shortened distinctly compared with normal group ［(61.83±4.13) vs. (72.70±7.05) ms, P<0.05］. The expression of TNF-α, IL-1 and IL-6 in plasma of model group were higher than normal group (P<0.05). High dose of HYY-002 (10 mg/kg) shortened AF duration effectively ［(6.42±1.38) vs. (16.32±1.31) s，P<0.01 vs. model group］, relieved the shortening of AERP induced by AF ［(77.78±3.79) vs. (61.83±4.13) ms, P<0.01 vs. model group］ and lowered the inflammatory cytokines level in plasma. Compared with normal group, the expression of miR-135a in plasma of model group was down-regulated obviously (P<0.01). CONCLUSION: HYY-002 has a significant therapeutic effect on AF, and miR-135a might be involved in the development of AF.

Mechanism of total flavonoids of Rhododendron blocking Rho kinase-induced vasodilation of coronary artery in rats

LI Yanan, CHEN Zhiwu, GUO Yan

2019, 24(12):  1353-1357.  doi:10.12092/j.issn.1009-2501.2019.12.006

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AIM: To investigate the mechanism of total flavonoids of Rhododendron blocking Rho kinase-induced vasodilation of coronary artery in rats. METHODS: ROCK1-siRNA and ROCK2-siRNA rats were prepared by siRNA technique. ROCK1 and ROCK2 of coronary artery were measured by western-blot. Coronary artery tension was measured by a microvascular tension system. The diastolic function of normal and interfered vascular was detected with Y27632 and TFR. RESULTS:Compared with control group, the expression of ROCK1in ROCK1-siRNA group and expression of ROCK2 in ROCK2-siRNA group were decreased, while the expression of ROCK1 and ROCK2 in negative siRNA and transfection reagent groups were not significant difference, siRNA interference technology can effectively reduce expression of ROCK1 and ROCK2 of coronary artery tissue.Compared with vehicle group, TFR and Y27632 can cause vasodilation in ROCK1-siRNA and ROCK2-siRNA transfected vascular. Compared with normal group, TFR and Y27632 significantly attenuated the vasodilation in ROCK1-siRNA and ROCK2-siRNA transfected vascular; The Emax of vasodilation which induced by TFR in ROCK2-siRNA group was higher than ROCK1-siRNA group.CONCLUSION: The vasodilation of coronary artery which induced by total flavonoids of Rhododendron on rats is associated with blocking ROCK and may selectively act on ROCK1.

Effects of curcumin on proliferation of VSMCs and expression of PTEN induced by PDGF-BB

QIU Fei, GAO Dan, YANG Dongmei, ZHONG Xiaomei, TANG Sha, YIN Huiming, ZHANG Zaiqi

2019, 24(12):  1358-1363.  doi:10.12092/j.issn.1009-2501.2019.12.007

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AIM: To study the effects of curcumin on the proliferation of vascular smooth muscle cells (VSMCs) and the deletion of phosphatase and tensin homology deletedon chromosome ten (PTEN) induced by platelet-derived growth factor-BB (PDGF-BB) and to provide more abundant experimental basis for the clinical application of Dong nationality medicine "Curcuma longa". METHODS: The proliferation model of VSMCs was established by incubating with PDGF-BB (20 ng/mL) for 24 h. The cell activity was observed by MTT and CCK-8, cell cycle and cell migration were detected by flow cytometry and cell scratch assay, respectively. The effects of PTEN mRNA, PTEN protein and phosphorylated PTEN (p-PTEN) protein were observed by RT-PCR and Western blot. RESULTS:10, 30 μmol/L of curcumin was significantly inhibited the proliferation and migration of VSMCs induced by PDGF-BB (20 ng/mL). 10 μmol/L curcumin was used as the optimum concentration, it could not only increase the ratio of G0/G1 phase and decrease the proportion of S phase, but also inhibit the migration of VSMCs. At the same time, it could up-regulate the expression of PTEN mRNA and PTEN protein, down-regulate the expression of p-PTEN protein. CONCLUSION: Curcumin can inhibit the proliferation and migration of VSMCs induced by PDGF-BB. The effect of curcumin on PTEN may be related to the up-regulation of PTEN mRNA and PTEN proteins, down-regulation of p-PTEN proteins.

Compound Qishao Jiangya tablet reduces blood pressure in mesenteric artery of SHR rats by decreasing the deposition of type Ⅰ and type III collagen

LI Hong, LIU Yeqian, GONG Shan, LIU Lin, ZENG Yong, CAI Xiao, WANG Yuhong, REN Weiqiong

2019, 24(12):  1364-1370.  doi:10.12092/j.issn.1009-2501.2019.12.008

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AIM: To explore the mechanism of compound Qishao Jiangya tablet on blood pressure and vascular remodeling in spontaneously hypertensive rats (SHR).  METHODS: SHR rats were randomly divided into model group, irbesartan tablet group and compound Qishao Jiangya tablet group, 10 rats in each group; Another 10 WKY rats were used as normal control group; All received administration for 6 weeks; noninvasive sphygmomanometer was used to measure the changes of blood pressure in rats; HE staining was used to observe the pathological changes of mesenteric artery in rats and to measure the thickness of mesenteric artery wall; The thickness of intima media and the diameter of lumen in the same position were recorded as WT; Detection of matrix metalloprotease-2 (MMP-2) and type Ⅰ and type III collagen (CO Ⅰ, CO III) protein expression in mesenteric artery was performed by immuno-histochemical method. RESULTS:After 6 weeks of administration, compared with the normal control group, the blood pressure of the model group was significantly higher than that of the control group (P<0.01), and the thickness of tube wall and WT value were increased (P<0.01 or P<0.05), the expression of MMP -2, I and III collagen in mesenteric artery increased significantly (P<0.01); Compared with model group, the blood pressure of the rats in the compound Qishao Jiangya tablet group was significantly lower than that in the control group (P<0.01), The thickness of tube wall and WT value decreased (P<0.05), the expression of MMP-2 and type Ⅰ and type III collagen in mesenteric artery was significantly decreased (P<0.05), and the pathological changes were improved. CONCLUSION: Compound Qishaojiang tablet can reduce blood pressure and improve vascular remodeling in SHR rats, the mechanism may be related to the decrease of MMP-2 expression and the deposition of type Ⅰ and type III collagen.

Expression and clinical significance of EZH2 and α-SMA in myocardium of patients with rheumatic heart disease with atrial fibrillation

XU Shengsong, TAO Hui, SHI Kaihu, DING Jifei

2019, 24(12):  1371-1375.  doi:10.12092/j.issn.1009-2501.2019.12.009

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AIM: To investigate the expression correlation between histone-lysine N-methyltransferase EZH2 and α-SMA in the patients with rheumatic heart disease and atrial fibrillation (AF). METHODS: Tissues of auricula dextra were removed from 20 patients with rheumatic heart disease undergoing cardiac surgery for correction to valvular defect. According to the definition of AF, 20 patients were divided into group of AF group and of sinus rhythm (SR) group (n=10). The collagen deposition in myocardial tissue was detected by Masson's trichrome stain. The expression of EZH2 and α-SMA were detected by immunohistochemistry, qRT-PCR and Western blot. RESULTS:Masson staining results revealed that the collagen deposition and the comparisons of CVF were significantly increased in the AF heart tissue compared with the SR control(P<0.05). Immunohistochemistry indicated that comparing with the SR group; the expressions of EZH2 and α-SMA protein were significantly increased in AF group (P<0.05). Western blot indicated that compared with the SR group, the expressions of EZH2 and α-SMA protein were significantly increased in AF group(P<0.05). Moreover, qRT-PCR found that compared with the SR group, the expressions of EZH2 and α-SMA mRNA were significantly increased in AF group(P<0.05). CONCLUSION: High expressions of EZH2 and α-SMA indicate EZH2 and α-SMA can regulate the development of AF.

Effects of adenosine A2A receptor antagonist on lipopolysaccharide induced inflammatory BV-2 microglial cells' morphology and function

CHEN Yu，YIN Weiyong，CHEN Yanyan，ZHU Zhenguo，ZHENG Rongyuan，ZHENG Liupu

2019, 24(12):  1376-1384.  doi:10.12092/j.issn.1009-2501.2019.12.010

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AIM: To investigate the therapeutic effects of adenosine A2A receptor antagonist on experimental autoimmune encephalomyelitis (EAE) and to explore the regulating effects on microglia morphology and function. METHODS: EAE model was induced by MOG35-55 in C57BL/6 mice. Adenosine A2AR antagonists were given by intraperitoneal injection as EAE mice showed neurobehavioral deficits. The treatment lasted ten days until EAE mice reached highest clinical score. ELISA method was used to detect the expression of pro-inflammatory cytokine in central nervous system; immunofluorescence double staining was used to detect M1 cell related markers and M2 cell related markers in microglia. In vitro, activated BV-2 microglia cell line was induced by lipopolysaccharide (LPS) and then was intervened by the A2AR antagonists. Real-time PCR and ELISA method were used to detect the M1 and M2 cells related cytokines. Western Blot method was used to detect the synthesis of M1 and M2 cell related markers. RESULTS:Adenosine A2AR antagonists can effectively ameliorate the EAE-induced neurobehavioral deficits when treated after onset of EAE, and can reduce the secretion of pro-inflammatory cytokine IFN-γ, and M1 cells related iNOS synthesis while increased M2 type cells related ArgI synthesis. Adenosine A2AR antagonists can reduce LPS-induced BV-2 M1 microglial cells related cytokines IL-1β, and had no influence on M2 cells related cytokines and protein. CONCLUSION: Adenosine A2AR antagonists have definite therapeutic effect on EAE mice when treated after the onset of EAE; its underlying mechanism may be involved with shift of phenotype (M1/M2) and changes in morphology and function of microglia during neuro-inflammatory process.

Ultrasound-microbubbles mediated microRNA-449a inhibits lung cancer cell growth via the regulation of Notch1

ZHU Linjia, YUAN Shaofei, SHANGGUAN Zongxiao, CI Xiao, ZHAO Renguo, LI Yuping

2019, 24(12):  1385-1393.  doi:10.12092/j.issn.1009-2501.2019.12.011

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AIM: The application of gene-loaded microbubbles (MBs) combined with ultrasound that results in increased delivery efficiency, may be an excellent method of gene delivery. This study aimed to discuss effects of ultrasound-MB mediated microRNA (miR)-449a on lung cancer (LC) development by targeting Notch1. METHODS: Initially, miR-449a expression in LC tissues, paracancerous tissues, LC cell lines and lung epithelial cells was detected and its association with LC patients' clinical characteristics was analyzed. The gain-of function studies were performed to probe the roles of miR-449a and ultrasound-MB mediated miR-449a in LC progression. Then RT-qPCR combined with Western blot analysis was applied to verify the levels of miR-449a, Notch1, proliferation- and apoptosis-related proteins. RESULTS:Poorly expressed miR-449a was observed in LC. Overexpression of miR-449a suppressed LC cell proliferation, promoted G2/M arrest and apoptosis. Ultrasound-MB-mediated miR-449a strengthened inhibitory effects of miR-449a on cell growth and resistance to apoptosis. miR-449a inhibited H1299 cell activity by targeting Notch1. CONCLUSION: Our data supported that miR-449a overexpression inhibited LC cell growth, and ultrasound-MB-mediated miR-449a reinforced the repressive effects of miR-449a on LC progression. This investigation may offer new insight for LC treatment.

Effect of miR-423-5p on the injury of AR42J cells induced by caerulein through targeting AQP1

LIAO Wei, TANG Yucheng, ZHOU Tingting, ZHOU Furong

2019, 24(12):  1394-1401.  doi:10.12092/j.issn.1009-2501.2019.12.012

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AIM: To investigate the effect of miR-423-5p on the injury of pancreatic AR42J cells induced by caerulein and explore the underlying molecular mechanism. METHODS: A model of pancreatitis injury was established by treating AR42J cells with caerulein. The expression level of miR-423-5p in AR42J cells was detected by qRT-PCR. The expression levels of aquaporin 1(AQP1), Bcl-2, Bax and capase3 were measured by Western blot. The levels of IL-6 and TNF-α in culture supernatants were detected by enzyme-linked immunosorbent assay (ELISA). The cell apoptotic rate was determined by flow cytometry. The relationship between miR-423-5p and AQP1 was verified by dual-luciferase reporter assay system. RESULTS:miR-423-5p was up-regulated and AQP1 was down-regulated in AR42J cells induced by caerulein. Inhibition of miR-423-5p or overexpression of AQP1 alleviated the injury of AR42J cells induced by caerulein and inhibited cell apoptosis. The results of dual-luciferase reporter assay system suggested that miR-423-5p targeted and negatively regulated the expression of AQP1. Inhibition of AQP1 reversed the effects of inhibition of miR-423-5p on the injury of AR42J cells induced by caerulein. CONCLUSION: miR-423-5p alleviates the injury of pancreatic AR42J cells induced by caerulein and inhibited apoptosis by targeting AQP1.

Molecular network regulation mechanism of Lycii Fructus in promoting directional differentiation of iris pigment epithelial cells to treat retinitis pigmentosa

SONG Houpan, ZENG Meiyan, CHEN Xiaojuan, CHEN Xinyi, PENG Jun, ZHOU Yasha, YANG Yijing, YANG Tao, CAI Xiong, PENG Qinghua

2019, 24(12):  1402-1414.  doi:10.12092/j.issn.1009-2501.2019.12.013

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AIM: To investigate the molecular network regulation mechanism of Lycii Fructus (LF) in promoting directional differentiation of iris pigment epithelial cells in the treatment of retinitis pigmentosa(RP) based on the methods of bioinformatics and network pharmacology. METHODS: The main active ingredients and potential targets of LF were retrieved from TCMSP database and analysis platform. The data of GSE81058 gene expression profile was downloaded from GEO database. Volcanic maps and clustering thermal maps of differentially expressed genes between IPE and RPE were plotted by ggplot2 and Pheatmap packages, respectively. Protein-protein interaction (PPI) networks of LF component-target and IPE-RPE differentially expressed genes were constructed by STRING database. Cytoscape software was used to extract genes of the intersection network. Gene ontology and signaling pathway analysis of intersection genes were carried out through DAVID online database. CytoHubba was used to analyze the key targets of LF. RESULTS:A total of 188 chemical constituents of LF were obtained, of which 36 were the main active ingredients in blood. There were 201 possible targets for these active ingredients. 142 differentially expressed genes of IPE and RPE were obtained, of which 71 were up-regulated and 71 were down-regulated. 105 gene targets related to LF promoting IPE differentiation and treating RP were identified. The biological processes involved in LF acting on these targets included regulating cell differentiation and retinal layer formation. The related molecular functions mainly involved transcriptional co-activator activity, ion channel activity, etc. They were mainly concentrated in cytoplasm, Golgi apparatus, and other areas. The molecular mechanisms involved the regulation of PI3K-Akt signaling pathway, neuroactive ligand-receptor interaction pathway, etc. The key targets of LF for IPE differentiation include SPP1, MMP9, SNAI2, etc.CONCLUSION: The gene expression profiles are of significant differences between IPE and RPE. The active ingredients of LF can act on these differentially expressed genes, promote IPE cells to differentiate into RPE, and thus treat RP. This study provides a scientific basis for the combination of cell transplantation and traditional Chinese medicine in the treatment of RP.

Clinical study on the blood conservation effect of different time application of tranexamic acid in patients with cardiac valve surgery undergoing cardiopulmonary bypass

YU Jun，JIN Xiaoju，GUO Jianrong，CAO Ya, LU Meijing, CHANG Yan, ZHOU Yumei, ZHOU Wei1

2019, 24(12):  1415-1420.  doi:10.12092/j.issn.1009-2501.2019.12.014

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AIM: To investigate the effect of different time of tranexamic acid on blood protection in patients undergoing cardiac valve replacement under the condition of cardiopulmonary bypass (CPB). METHODS: Forty patients undergoing cardiac valve replacement were randomly divided into two groups: group A (n=20) and group B (n=20). Group A received 15mg/kg tranexamic acid via central vein 5 minutes after heparinize. Group B received 15 mg/kg tranexamic acid intravenously 10 minutes after protamine injection at the end of cardiopulmonary bypass (CPB), and then 10 mg·kg-1·h-1 tranexamic acid was continuous intravenous infused until the end of the operation in the both groups. The venous blood samples were taken before operation T1, at the end of operation T2, and at the morning of after operation T3, 24 hours after operation T4. Then the coagulation indexes and the blood routine of the two groups were analyzed. The volume of pericardial mediastinal drainage, allogeneic erythrocyte red suspension and plasma input were recorded at T3 and T4. RESULTS:Compared with group B, group A could reduce pericardial mediastinal drainage and plasma infusion. But in terms of coagulation function, the APTT in group B at T3 time point was significantly longer than that in group A, the DD in group B at T2-4 time point and the FDP in group B at T2 time point was significantly higher than that in group A as well. No significant differences were found in all the other coagulation indexes (PT,APTT,INR,FIB,FDP) and blood routine (HB,HCT,PLT) between the two groups during perioperative period. There were no significant differences in the volume of allogeneic red suspension infusion between the two groups, but the volume of pericardial mediastinal drainage and the demand of allogeneic plasma in group B were significantly more than those in group A at T3-4. CONCLUSION:When tranexamic acid is intravenous medicated before CPB in patients undergoing cardiac valve replacement, tranexamic acid can reduce postoperative pericardial mediastinal drainage and allogeneic plasma infusion, and better inhibit hyperfibrinolysis.

Clinical observation of tocilizumab and etanercept for polyarticular course juvenile idiopathic arthritis

ZOU Lixia,LU Meiping,XU Yiping,ZHENG Qi,ZHENG Rongjun

2019, 24(12):  1421-1427.  doi:10.12092/j.issn.1009-2501.2019.12.015

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AIM: To observe and evaluate the clinical effect, immunomodulatory and safety of the tocilizumab and etanercept for patients with polyarticular juvenile idiopathic arthritis（pJIA). METHODS: Twenty-four pJIA patients of high disease activity were admitted from January 2017 to March 2019.All patients were divided into the tocilizumab group(12 cases)and the etanercept group(12 cases).Improvements of clinical symptoms, laboratory parameters and adverse reactions were evaluated and compared between these two groups at pretherapy and 3,6,12 months after the primary treatment. RESULTS:Compared with before treatment, the number of joint swelling, joint tenderness or pain during movement, C-reactive protein (CRP),erythrocyte sedimentation rate (ESR) and JADAS 27 scores in the tocilizumab group and the etanercept group were significantly improved (P<0.05) at 3 months after treatment. Moreover, CRP, ESR and JADAS 27 scores of the tocilizumab group decreased more significantly than those of the etanercept group (P<0.05).Compared with before treatment, the proportion of CD19+B and CD4+T cells, the decrease of IgG, IgA, IgM, C3, C4 and the proportion of CD8+T cells in the tocilizumab group were statistically significantat 6 months after treatment; IgG and IgA in the etanercept group were significantly lower than before treatment; IgG, IgA, IgM, C3, and C4 in the tocilizumab group were significantly lower than those of the etanercept group (P<0.05). At 12 months of treatment, the low disease activity rates of JADAS 27 in the tocilizumab group and the etanercept group were 36.4% and 37.5%, respectively; the ACR Pedi 30/50/70/90 in the two groups reached 100%/100%/87.5%/62.5% and 100%/100%/81.9%/45.5% relief. The most common adverse reaction was infection; meanwhile no significant adverse event happened. CONCLUSION:Tocilizumab and etanercept are effective for pJIA. Tocilizumab can quickly reduce the inflammatory parameters, improve disease activity, and regulate CD4+ T,CD19+ B cells.

Research progress on pathology mechanism and treatment target for diabetic sarcopenia

DING Fan, LI Wenxiong, ZHANG Jiali, ZHANG Yan

2019, 24(12):  1428-1433.  doi:10.12092/j.issn.1009-2501.2019.12.016

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Diabetes is a kind of metabolic diseases characterized by hyperglycemia. Sarcopenia is one of the common diabetic complications. Development of diabetic sarcopenia is related to ubiquitin-proteasome system,insulin resistance,oxidative stress,mitochondria damage,insulin signaling pathway and advanced glycationend products.This review summarized the pathological mechanism and treatment targets for diabetic sarcopenia based on national and international literatures.

Epigenetic regulation of Dapper family proteins in cancer

WU Juan, WU Yongjun, LI Zhi, ZENG Chang, LI Zhenfeng, TANG Yi, LU Miao, ZHANG Xuechun, ZHANG Wanyong, WANG Danhui, LIU Chenrui

2019, 24(12):  1434-1440.  doi:10.12092/j.issn.1009-2501.2019.12.017

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Dapper family proteins regulate the Wnt signaling pathway and are closely related to cancer initiation and progression. Dapper proteins usually are highly expressed in the normal tissues but often reduced or completely lost in tumors.S uch reduction in expression is mediated by the epigenetic regulation and associated with pathological characteristics, cancer progression and prognosis. Here we review the most recent discoveries in biological functions of Dapper family proteins in cancer initiation and progression as well as the mechanism underlying the epigenetic regulation of the expression of Dapper family proteins.